Chapter 26: The Urinary System Part 2 Flashcards
3 processes are involved in urine formation and adjustment of blood composition:
- Glomerular Filtration
- Tubular Reabsorption
- Tubular Secretion
Glomerular Filtration
is a passive and nonselective process (no metabolic energy required)
• Hydrostatic pressure forces fluids and solutes through filtration membrane into glomerular capsule
• No reabsorption into capillaries of glomerulus occur
Tubular Reabsorption
selectively returns 99% of substances from filtrate to blood in renal tubules and collecting ducts
Tubular Secretion
- reabsorption in reverse
- primarily occurs in the distal convoluted tubule when active transport moves substances like creatine and penicillin, from the blood into this tubule.
- disposes of unwanted solutes, eliminates solutes that were reabsorbed, rids the body of excess K+, and controls blood pH.
- Tubular secretion is most active in the proximal convoluted tubule, but occurs in the collecting ducts and distal convoluted tubules, as well.
Glomerular Blood Hydrostatic Pressure (GBHP) or Hydrostatic Pressure in Glomerular Capillaries (HPgc)
- It is the pressure of blood in the glomerular capillaries
- Chief force pushing water & solutes out of blood
- Glomerular Blood Pressure: 55 mmHg
Capsular Hydrostatic Pressure (CHP) or Hydrostatic pressure in capsular space (HPcs)
- Opposing force to GBHP by fluid already in the capsular space that tends to push water and solutes out of the filtrate and back into plasma
- results from the resistance to flow along the nephron and conducting system
- Filtrate Pressure in Capsule: 15 mm Hg
Blood Colloid Osmotic Pressure (BCOP) or Colloid osmotic pressure in capillaries (OPgc)
- pressure exerted by the proteins in the plasma which tends to retain fluid and also oppose filtration
- pulls fluid into capillaries from interstitial spaces
- “Pull” of Proteins in Blood: 30 mm Hg
Explain what is meant from NFP
Net Filtration Pressure (NFP): sum of forces
• Pressure responsible for filtrate formation
• Main controllable factor determining Glomerular Filtration Rate (GFR)
How is Net Filtration Pressure calculated?
NFP = GBHP (outward pressures) - (CHP + BCOP) (inward pressures)
= 55 - (15 + 30) -> NFP = 10 mm Hg
What forces determine filtration pressure?
- Glomerular (blood) hydrostatic pressure GHP or GBHP
- Capsular Hydrostatic Pressure (CHP)
- (Blood) Colloid Osmotic Pressure (BCOP)
Glomerular Filtration Rate (GFR) is influenced by
- Net filtration pressure
- Total surface area for filtration
- filtration membrane permeability
What is the relationship between glomerular filtration rate (GFR) and NFP?
- Primary factor that influences GFR (primary pressure is glomerular blood hydrostatic pressure (GBHP)
- Increase NFP = Increase GFR (directly proportional)
How does total surface area for filtration influence the rate of glomerular filtration rate?
Glomerular mesangial cells control by contracting
How does filtration membrane permeability influence glomerular filtration rate?
Much more permeable than other capillaries
How is GFR regulated?
- intrinsic controls (renal autoregulation)
2. extrinsic controls
Why is it important to maintain a constant GFR?
Constant GFR is important as it allows kidneys to make filtrate and maintain extracellular homeostasis
Increased GFR causes
increased urine output, which lowers blood pressure, and vice versa
Intrinsic Controls: Renal Autoregulation of GFR
-Main goal is to maintain GFR in the kidney
-Maintains nearly constant GFR when MAP is in range of 80–180 mm Hg
• Autoregulation stops if out of that range
2 Types of Renal Autoregulation:
- Myogenic Mechanism
2. Tubuloglomerular Feedback Mechanism
Myogenic Mechanism
Local smooth muscle (walls of afferent arteriole) contracts when stretched
– Increased MAP or Decreased MAP
Both help maintain normal GFR despite normal fluctuations in systemic blood pressure (MAP)
What happens when MAP is increased during the myogenic mechanism?
constriction of afferent arterioles:
- Reduces blood flow into glomerulus -> decreases GBHP
- Protects glomeruli from damaging high BP
What happens when MAP is decreased during the myogenic mechanism?
dilation of afferent arterioles:
-Increases blood flow into glomerulus -> increases GBHP
Tubuloglomerular Feedback Mechanism
Flow-dependent mechanism directed by macula densa cells of JGA
- Respond to: - filtrate’s NaCl concentration (filtrate’s osmolarity) &/or - flow of filtrate in renal tubules
Extrinsic Controls
– Purpose of extrinsic controls is to regulate GFR to maintain systemic blood pressure
– Extrinsic controls will override renal intrinsic controls if blood volume needs to be increase
What mechanisms do extrinsic controls use?
- Neural Mechanisms
2. Hormonal Mechanisms
Neural Mechanisms
Sympathetic Nervous System
• During Rest:
– Renal blood vessels (including afferent & efferent arterioles): dilate
– Renal autoregulation mechanisms prevail
• During Stress or Emergency: Low BP/blood volume (blood loss; excessive fluid loss – chronic diarrhea, frequent vomiting; dehydration) or High BP (exercise)
– Norepinephrine is released by sympathetic nervous system and epinephrine is released by adrenal
medulla
Release of norepinephrine and epinephrine by neural mechanisms causes
- Systemic vasoconstriction (including renal blood vessels): increases blood pressure, and reduces blood flow to the kidneys
- Strong constriction of afferent arterioles: significantly decreases GFR (decrease in urine output)
- Blood Volume and Blood Pressure: Increase
Hormonal Mechanisms
- Atrial Natriuretic Peptide (ANP)
2. Renin-Angiotensin-Aldosterone System (RAAS)
Atrial Natriuretic Peptide (ANP)
- released by cells of the atria when blood pressure/blood volume increases
- causes relaxation of glomerular mesangial cells -> increases capillary surface area -> increases GFR
Renin-Angiotensin-Aldosterone System (RAAS)
- when blood pressure/blood volume decreases -> main mechanism for increasing blood pressure/blood volum
3 Pathways to Renin release by Juxtaglomerular Cells (Granular Cells):
- Direct stimulation of granular cells by sympathetic nervous system
- Stimulation by activated macula densa cells when filtrate NaCl concentration is low
- Reduced stretch of granular cells
Anuria
abnormally low urinary output (less than 50 ml/day)
• May indicate that glomerular blood pressure is too low to cause filtration
• Renal failure and anuria can also result from situations in which nephrons stop functioning
– Example: acute nephritis, transfusion reactions, and crush injuries
What are the two routes of tubular reabsorption?
- transcellular route
2. paracellular route
Transcellular Route (Transcellular Reabsorption)
- Solute enters apical membrane of tubule cells
- Travels through cytosol of tubule cells
- Exits basolateral membrane of tubule cells
- Enters blood through endothelium of peritubular capillaries
Paracellular Route (Paracellular Reabsorption)
Between tubule cells
– Limited by tight junctions, but leaky in PCT
» Water, Ca2+, Mg2+, K+, and some Na+ in the PCT move via this route
Proximal Convoluted Tubule (PCT)
– Site of most reabsorption:
• All nutrients, such as glucose and amino acids, are 100% reabsorbed
• 65% of Na+, K+ and water reabsorbed
• Many ions (passive diffusion): 50% Cl-, 80% - 90% bicarbonate, variable amounts of calcium and phosphate • 50% of urea
Tubular Reabsorption of Sodium
- transported across apical membrane
2. transported across basolateral membrane
What happens to sodium as it is transported across the apical membrane?
Na+ enters tubule cell at apical surface via secondary active transport (cotransport) or via facilitated diffusion through channels:
- Active pumping of Na+ at basolateral membrane results in strong electrochemical gradient within tubule cell
– Results in low intracellular Na+ levels that facilitates Na+ diffusion
Sodium transported across basolateral membrane
– Na+ is most abundant cation in filtrate
– Transport of Na+ across basolateral membrane of tubule cell is via primary active transport
– Na+-K+ ATPase pumps Na+ into interstitial space
– Na+ is then swept by bulk flow into peritubular capillaries